Loss of heterozygosity on chromosome 9 in human breast cancer: Association with clinical variables and genetic changes at other chromosome regions

Eiríksdóttir, Guðný; Sigurðsson, Ásgeir; Jonasson, Jón G.; Agnarsson, Bjarni A.; Sigurðsson, Helgi; Guðmundsson, Jūlı́us; Bergþórsson, Jón Þór; Barkardóttir, Rósa B.; Egilsson, Valgarður; Ingvarsson, Sigurður

doi:10.1002/ijc.2910640605

Cited by 34 publications

(22 citation statements)

References 11 publications

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“…BRG1 is located in or near several microsatellite markers that demonstrate loss of heterozygosity in human cancers (Medina et al, 2004;Gunduz et al, 2005), and the BRM locus is a site of loss of heterozygosity in human cancers as well (Eiriksdottir et al, 1995;Neville et al, 1995;An et al, 1999;Jin et al, 1999;Sarkar et al, 2002;Tripathi et al, 2003;Sabah et al, 2005). About 26% of small-cell lung cancer cell lines and 76% of non-small-cell lung cancer cell lines have loss of heterozygosity at D9S288, which is in proximity to the BRM gene (Girard et al, 2000).…”

Section: Loss Of Heterozygosity Occurs At the Brg1 And Brm Locimentioning

confidence: 99%

The SWI/SNF complex and cancer

2009

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The mammalian SWI/SNF complexes mediate ATPdependent chromatin remodeling processes that are critical for differentiation and proliferation. Not surprisingly, loss of SWI/SNF function has been associated with malignant transformation, and a substantial body of evidence indicates that several components of the SWI/SNF complexes function as tumor suppressors. This review summarizes the evidence that underlies this conclusion, with particular emphasis upon the two catalytic subunits of the SWI/SNF complexes, BRM, the mammalian ortholog of SWI2/SNF2 in yeast and brahma in Drosophila, and Brahma-related gene-1 (BRG1).

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Section: Loss Of Heterozygosity Occurs At the Brg1 And Brm Locimentioning

confidence: 99%

The SWI/SNF complex and cancer

2009

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“…The number of allelic imbalance events detected for somatic genetic events, such as loss of heterozygosity, during E2-induced mammary carcinogenesis (Callahan each of the markers assayed on RNO18 varied from 4 to 11 (19 to 52%; Figure 5). Twenty-two of the 30 (73%) et al 1992; Bieche and Lidereau 1995; Eiriksdottir et al 1995;Weith et al 1996;Tirkkonen et al 1998; allelic imbalance events detected represented either loss of the COP resistance allele or gain of the susceptible An et al 1999;Loveday et al 2000;Richard et al 2000). Frequent somatic loss would suggest that these Emca ACI allele.…”

Section: D5rat30mentioning

confidence: 99%

Genetic Determination of Susceptibility to Estrogen-Induced Mammary Cancer in the ACI Rat

et al. 2004

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Hormonal, genetic, and environmental factors play major roles in the complex etiology of breast cancer. When treated continuously with 17␤-estradiol (E2), the ACI rat exhibits a genetically conferred propensity to develop mammary cancer. The susceptibility of the ACI rat to E2-induced mammary cancer appears to segregate as an incompletely dominant trait in crosses to the resistant Copenhagen (COP) strain. In both (ACI ϫ COP)F 2 and (COP ϫ ACI)F 2 populations, we find strong evidence for a major genetic determinant of susceptibility to E2-induced mammary cancer on distal rat chromosome 5. Our data are most consistent with a model in which the ACI allele of this locus, termed Emca1 (e strogen-induced m ammary ca ncer 1), acts in an incompletely dominant manner to increase both tumor incidence and tumor multiplicity as well as to reduce tumor latency in these populations. We also find evidence suggestive of a second locus, Emca2, on chromosome 18 in the (ACI ϫ COP)F 2 population. The ACI allele of Emca2 acts in a dominant manner to increase incidence and decrease latency. Together, Emca1 and Emca2 act independently to modify susceptibility to E2-induced mammary cancer.

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“…Previous studies (Devilee et al, 1991;Eiriksdottir et al, 1995;Kerangueven et al, 1995;Koreth et al, 1997) described losses of heterozygosity (LOH) in breast cancer in a high percentage at lp, 6q, 9p, llq, 13q and 16q. In general, these allelic losses correspond well to the most frequent DNA underrepresentations found in our study.…”

Section: Dna Lossesmentioning

confidence: 99%

Chromosome alterations in breast carcinomas: frequent involvement of DNA losses including chromosomes 4q and 21q

Schwendel

Richard²,

Langreck³

et al. 1998

Br J Cancer

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Summary Comparative genomic hybridization was applied to map DNA gains and losses in 39 invasive ductal breast carcinomas. Frequent abnormalities included gains on chromosomal regions lq, 8q, 11q12-13, 16p, 19, 20q and X as well as frequent losses on 1 p, 5q, 6q, 9p, llq, 13q and 16q. Furthermore, frequent losses on 4q (20 cases) and 21q (14 cases) were found for the first time in this tumour type. High copy number amplifications were observed at 8q12-24, 11qll-13 and 20q13-ter. Highly differentiated tumours were associated with gains on 1q and 11q12-13 along with losses on 1p21-22, 4q, 13q, 11q21-ter. Undifferentiated breast carcinomas were characterized by additional DNA imbalances, i.e. deletions of 5q13-23, all of chromosome 9, the centromeric part of chromosome 13 including band 13q14 and the overrepresentation of chromosome X. We speculate that these changes are associated with tumour progression of invasive ductal breast cancer.

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Loss of heterozygosity on chromosome 9 in human breast cancer: Association with clinical variables and genetic changes at other chromosome regions

Cited by 34 publications

References 11 publications

The SWI/SNF complex and cancer

The SWI/SNF complex and cancer

Genetic Determination of Susceptibility to Estrogen-Induced Mammary Cancer in the ACI Rat

Chromosome alterations in breast carcinomas: frequent involvement of DNA losses including chromosomes 4q and 21q

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